Semin Musculoskelet Radiol 2002; 06(3): 173-182
DOI: 10.1055/s-2002-36714
Copyright © 2002 by Thieme Medical Publishers, Inc., 333 Seventh Avenue, New York, NY 10001, USA. Tel.: +1(212) 584-4662

Vitamin D Metabolism, Rickets, and Osteomalacia

Jacqueline L. Berry, Michael Davies, Andrew P. Mee
  • Vitamin D Research Group, University School of Medicine, Manchester Royal Infirmary, Manchester, United Kingdom
Further Information

Publication History

Publication Date:
23 January 2003 (online)

ABSTRACT

Rickets in the growing child or adolescent and osteomalacia in the adult develop in a variety of clinical situations and have in common an absence or delay in the mineralization of growth cartilage and in newly formed bone collagen. Classically, deficiency of vitamin D, which is essential for the absorption of dietary calcium, has been the major cause. However, rickets is also seen as a result of hereditary defects in critical vitamin D signaling molecules. Disturbances of phosphate metabolism can also lead to signs of rickets and osteomalacia, notably X-linked hypophosphatemic rickets, and oncogenic osteomalacia. Extrarenal synthesis of 1,25-dihydroxyvitamin D, such as that associated with granulomatous disease, can also lead to disturbances in calcium metabolism, with associated skeletal and nonskeletal changes.

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